Chlamydophila Pneumoniae Infection association w/ Heart Disease

chlamydophila and heart disease

 

By Jay A. Glasel, PH.D.

Managing Member

Global Scientific Consulting, LLC

Coronary heart disease (CHD) is the leading cause of death in the developed world with an estimated 3.8 million men and 3.4 million women dying each year. CHD is characterized by the narrowing or blockage of the coronary arteries, usually caused by atherosclerosis due to buildup of fatty material and plaque. This atherosclerotic pathological process in the walls of blood vessels is complex and develops over many years.

From what we’ve read in newspapers and magazines and heard from our doctors, “risk factors” combine to cause CHD: smoking, alcohol, some foods, lack of exercise and so forth. But it is known in the medical community that these risk factors have not adequately explained the worldwide trends and incidence of CHD and this fact has led to searches for other risk factors or causes.

This article is about what many scientists believe is another significant risk factor for CHD. This risk factor—a common bacterial infection of humans—has been the subject of scientific research in many laboratories for several decades but the research has so far generated more debate than definitive answers. The story of understanding this risk factor research illustrates the fiendishly difficult problem in dealing with many human diseases—separating what causes a particular disease from other conditions that are just correlated with the disease.

The story goes back more than a century. In the early days of scientific medicine it was suggested that the pathogenic mechanism of CHD might be an increased inflammatory response in arterial tissue due to infections. For a review of this history see [1].

For various reasons this explanation of CHD caused by infectious disease lost favor in medical opinion to today’s widely accepted concept of non-infectious risk factors. But there have always been dissenters who believe that infectious disease plays a role in CHD.

These dissenting opinions were first based on epidemiological evidence that appeared after the beginning widespread use of antibiotics in the late 1940s. In particular, throughout the world epidemiologists observed that the incidence of heart disease began to fall in populations where smoking and other non-infectious risk factors were still widespread but where antibiotics were also widely used.

If infections are a factor in CHD it is logical to look for those that are common in populations. And in the mid-1970s into the 1980s some medical researchers took up this challenge.

Scientific papers in began to appear in increasing numbers linking infections caused by a small bacterium named Chlamydia pneumoniae to CHD. (A more recently used, but not universally accepted, name for the bacterium is Chlamydophila pneumoniae. To avoid confusion the shortened name C. pneumoniae is used here.) Note that this bacterium is not the Chlamydia species involved in sexually transmitted disease. C. pneumoniae is transmitted via airborne means.

C. pneumoniae infections are very common in human populations. Antibodies against the bacterium have a prevalence of 50% by age 20 years and 70–80% at age 60–70 years. Infection by this bacterium is a cause of community-acquired pneumonia, pharyngitis, bronchitis, sinusitis, and worsening of chronic bronchitis and asthma.

Since the 1980s almost 1700 scientific papers have reported research that link C. pneumoniae infection to CHD. The research described in these papers demonstrated that animals (rabbits, mice) deliberately infected with C. pneumoniae developed atherosclerosis and that plaque formation in animal models could be decreased by an antibiotic active against C. pneumoniae. Other research showed that a high percentage of plaques in the arteries of humans who had died of CHD contained evidence of past or present C. pneumoniae infection. And in 2001-2002 research was reported that showed that in a strain of mice that spontaneously develop atherosclerosis, chronic C. pneumoniae infection increased plaque sizes.

This research caused excitement and debate in the medical community. The excitement was due to the possibility of reducing the incidence of CHD in human populations by the use of antibiotics. The debate was whether C. pneumoniae infections are correlated with CHD or are they causes of CHD. That is, does C. pneumoniae just happen to be present in a lot of CHD patients and has nothing or little to do with the development of arterial inflammation?

In the period 2001-2004 small clinical trials were performed where patients with CHD were administered an antibiotic that targeted C. pneumoniae. The results showed a decrease in heart attacks and death in these groups of patients. Obviously, more rigorous and larger scale clinical trials were called for.

To determine the effects of antibiotic treatments against C. pneumoniae on reduction of CHD in patients, about 20 large scale randomized trials that included thousands of patients were performed in the early 2000s. Combined analyses of the results of all these trials showed that antibiotic treatment had absolutely no effect on any aspect of CHD or on all-cause mortality. For a review of this part of the story see [2].

Following the publication of these negative results in 2004-2005 research into the role of C. pneumoniae in CHD dropped dramatically as evidenced by the sharp decrease in the number of papers published. But the question that has lingered on for more than a decade since is: Did these clinical trials really rule out C. pneumoniae infection as an important risk factor in CHD? The answer in the minds of some involved researchers is no [3].

The basic criticism of the large scale anti-C. pneumoniae trials is that the development of arterial inflammation by C. pneumoniae infection is a long-term process possibly extending from childhood while the trials involved only a few years’ treatment with antibiotics. If this criticism is accepted, the only way to truly find out if C. pneumoniae infections are causal in CHD would be a very expensive and lengthy family-based study to link atherosclerotic lesion development to degree of C. pneumoniae infection [3].

So we are left with this: A possibly important causal contributor to CHD has fallen out of clinical consideration because of dramatically negative clinical trial results. However, the trial designs have been criticized and the negative results could be very misleading. So the question of cause or correlation involving C. pneumoniae infection and CHD is still very much up in the air and the only way to resolve the question would be a very expensive and lengthy clinical study. How much are developed societies willing to expend in time and money to find additional risk factors to their most deadly disease?

References

1. Nieto, F.J., Infections and atherosclerosis: new clues from an old hypothesis? Am J Epidemiol, 1998. 148(10): p. 937-48. (Available to Download On-line)

2. Epstein, S.E., et al., Insights into the role of infection in atherogenesis and in plaque rupture. Circulation, 2009. 119(24): p. 3133-41. (Available to Download On-line)

3. Grayston, J.T., et al., Infection with Chlamydia pneumoniae as a cause of coronary heart disease: the hypothesis is still untested. Pathog Dis, 2015. 73(1): p. 1-9. (Available to Download O


Tags: chlamydophila , chlamydophila pneumoniae infection , correlation of chlamydophila and CHD , CHD , Jay Glasel

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